Several decades ago, the severity of heart failure was gauged according to a depression in myocardial contractility, defined as that biochemical property of cardiac muscle that determines the extent of shortening independent of its initial length and the load against which it shortens. Mathematical models were used to derive indices of contractility (1). These theoretical constructs included a contractile element tethered to elastic elements that were situated both in series and in parallel to it. Cardiomyocytes, with their actin and myosin protein microfilaments, constitute the myocardium’s contractile elements, whereas fibrillar collagen is the anatomic correlate of these elastic elements.